Mitochondrial Reprogramming induced by CaMKIIδmediates hypertrophy decompensation

Autor: Daan Westenbrink, B, Ling, H, Divakaruni, AS, Gray, CBB, Zambon, AC, Dalton, ND, Peterson, KL, Gu, Y, Matkovich, SJ, Murphy, AN, Miyamoto, S, Dorn, GW, Brown, JH

Publikováno v: Daan Westenbrink, B; Ling, H; Divakaruni, AS; Gray, CBB; Zambon, AC; Dalton, ND; et al.(2015). Mitochondrial Reprogramming induced by CaMKIIδmediates hypertrophy decompensation. Circulation Research, 116(5), e28-e39. doi: 10.1161/CIRCRESAHA.116.304682. UCLA: Retrieved from: http://www.escholarship.org/uc/item/4mm9j470

© 2015 American Heart Association, Inc. Rationale: Sustained activation of Gαq transgenic (Gq) signaling during pressure overload causes cardiac hypertrophy that ultimately progresses to dilated cardiomyopathy. The molecular events that drive hyper

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=od_______325::e5a11b9acbc074d26f3a5c984b6be45c
http://www.escholarship.org/uc/item/4mm9j470

Akt regulates L-type Ca2+channel activity by modulating Cavα1 protein stability

Autor: Catalucci, D, Zhang, DH, Desantiago, J, Aimond, F, Barbara, G, Chemin, J, Bonci, D, Picht, E, Rusconi, F, Dalton, ND, Peterson, KL, Richard, S, Bers, DM, Brown, JH, Condorelli, G

Publikováno v: Catalucci, D; Zhang, DH; Desantiago, J; Aimond, F; Barbara, G; Chemin, J; et al.(2009). Akt regulates L-type Ca2+channel activity by modulating Cavα1 protein stability. Journal of Cell Biology, 184(6), 923-933. doi: 10.1083/jcb.200805063. UC Davis: Retrieved from: http://www.escholarship.org/uc/item/7mk8j3s4

The insulin IGF-1 -PI3K-Akt signaling pathway has been suggested to improve cardiac inotropism and increase Ca2+handling through the effects of the protein kinase Akt. However, the underlying molecular mechanisms remain largely unknown. In this study

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4c9a4ca8d7eb93e290af04e5a14b7f50
https://doi.org/10.1085/jgp1334oia4

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